ArticleMolecular and cellular biology2004
Inactivation of the Mgat1 gene in oocytes impairs oogenesis, but embryos lacking complex and hybrid N-glycans develop and implant.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 92 citations in OpenAlex.
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- Rapid ovarian transcript changes during the onset of premature ovarian insufficiency.Reproduction & fertility · 2022Article
- Mouse Cre drivers: tools for studying disorders of the human female neuroendocrine-reproductive axis†.Biology of reproduction · 2022Review
- Deletion of Orc4 during oogenesis severely reduces polar body extrusion and blocks zygotic DNA replication†.Biology of reproduction · 2022Article
- Mouse zona pellucida proteins as receptors for binding of sperm to eggs.Trends in developmental biology · 2022Article
- Oocyte-specific disruption of adrenomedullin 2 gene enhances ovarian follicle growth after superovulation.Frontiers in endocrinology · 2022Article
- Diversity of sialic acids and sialoglycoproteins in gametes and at fertilization.Frontiers in cell and developmental biology · 2022Review
- Knockin' on Egg's Door: Maternal Control of Egg Activation That Influences Cortical Granule Exocytosis in Animal Species.Frontiers in cell and developmental biology · 2021Review
- Mammalian egg coat modifications and the block to polyspermy.Molecular reproduction and development · 2020Review
- 3D Structure and Function of Glycosyltransferases Involved inInternational journal of molecular sciences · 2020Review
- Roles for Golgi Glycans in Oogenesis and Spermatogenesis.Frontiers in cell and developmental biology · 2019Review
- Glycan-Independent Gamete Recognition Triggers Egg Zinc Sparks and ZP2 Cleavage to Prevent Polyspermy.Developmental cell · 2018Article
- More than just sugars: Conserved oligomeric Golgi complex deficiency causes glycosylation-independent cellular defects.Traffic (Copenhagen, Denmark) · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Complex and hybrid N-glycans contain sugar residues that have been implicated in fertilization, compaction of the embryo, and implantation. Inactivation of the Mgat1 gene responsible for their synthesis is embryonic lethal, but homozygous mutant blastocysts are phenotypically normal due to the presence of maternal Mgat1 gene transcripts. To identify roles for complex and hybrid N-glycans in oogenesis and preimplantation development, the Mgat1 gene in oocytes was deleted by using a ZP3Cre recombinase transgene. All mutant oocytes had an altered zona pellucida (ZP) that was thinner than the control ZP, and they did not possess complex N-glycans but contained ZP1, ZP2, and ZP3 glycoproteins. Mutant eggs were fertilized, all embryos implanted, and heterozygotes developed to birth. However, mutant females had decreased fertility, yielded fewer eggs after stimulation with gonadotropins, and produced a reduced number of preimplantation embryos and less progeny than controls. About 25% of embryonic day 3.5 (E3.5) embryos derived from mutant eggs were severely retarded in development, even when they were heterozygous and expressed complex N-glycans. Thus, a proportion of Mgat1(-)(/)(-) oocytes were developmentally compromised. Surprisingly, mutant eggs also gave rise to Mgat1(-)(/)(-) embryos that developed normally, implanted, and progressed to E9.5. Therefore, complex or hybrid N-glycans are required at some stage of oogenesis for the generation of a developmentally competent oocyte, but fertilization, blastogenesis, and implantation may proceed in their absence.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.